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56 Cards in this Set
- Front
- Back
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Rifamate
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-Isoniazid 150mg
-Rifampin 300mg |
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Rifater
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-Isoniazid 50mg
-Rifampin 120mg -Pyrazinamide 300mg |
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Drug Activity vs Fast Growing TB Subpopulations
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INH>RFM>STR>others (quinolones/EMB)
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Drug Activity vs Slow Growing TB Subpopulations
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PZA>INH>RFM
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First Line Agents vs. TB
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-Isoniazid (INH): IV/PO
-Rifampin (RFM): IV/PO -Pyrazinamide (PZA): PO -Ethambutol (EMB): PO -Streptomycin (STR): IM |
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Fluoroquinolone MOA
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-inhibition of topoisomerase II, aka DNA gyrase (gram -), and topoisomerase IV (gram +)
-bacteriacidal |
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Mechanism of Resistance vs. Fluoroquinolones
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-alterations of amino acid sequences which change base pairs of DNA decreasing the affinity for drug binding
-DNA gyrase (topoisomerase II) & topoisomerase IV mutations -decreased intracelluar accumulation |
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Fluroquinolone Gram - Activity
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-E. coli
-Enterobacteriaceae (E. coli, Klebsiella pneumoniae, Serratia marescens, Salmonella sp.) -Pseudomonas aeruginosa -Haemophilus influenzae -Moraxella catarrhalis -Neisseria gonorrhea |
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Fluroquinolone Limited Gram + Activity
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-Streptococcus pneumoniae
-Staphylococcus aureus -Enterococci sp. |
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Fluroquinolone Expanded Gram + Activity (Levofloxacin, Moxifloxacin, Gemifloxaxin)
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-PCN-R Streptococcus pneumoniae
-Streptococcus pyogenes -Atypicals (Legionella sp., Mycoplasma pneumoniae, Chlamydia pneumoniae) |
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Fluoroquinolone Anaerobic Activity (Levofloxacin, Moxifloxacin)
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-Bacteroides fragilis
-Provetella sp. -Fusobacterium sp. -Peptostreptococcus sp. -Clostridium sp. |
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DNA Gyrase (Topoisomerase II) Mutations
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-gyr A
-gyr B |
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Topoisomerase IV Mutations
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-par C
-par E |
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Reasons for Decreased Intracellular Fluoroquinolone Accumulation
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-reduced penetration thru cell wall
-active efflux |
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Use of Fluoroquinolones
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-UTI (not moxifloxacin)
-cSSSI -Infectious diarrhea -Urethral/cervical infections -Prostatis -Acute sinusitis -Acute exacerbations of chronic bronchitis -Community acquired pneumonia |
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Systemic Mycoses (Endemic Fungi)
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-Histoplasmosis (Histoplasma capsulatum)
-Blastomycoses (Blastomyces dermatophytosis) -Coccidioidomycosis (Coccidioides immitis) |
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Opportunistic Systemic Mycoses
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-Candidiasis (yeast)
-Cryptococcosis (yeast) -Aspergillosis (mould) -Zygomycoses (mould) |
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Polyenes MOA
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binds to ergosterol (more avidly then cholesterol), causing intercalation of cell membrane allowing leakage of intracellular cations
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When would you use Amphotericin B po?
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decontaminate gut prior to surgery
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Amphotericin B Resistance
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-Candida lusitaniae
-Aspergillus terreus -Scedosporium sp. -(+/-) Fusarium -Zygomycosis |
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Distribution of Amphotericin B to Tissue
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kidney>liver>spleen>lung>
heart>skeletal muscles>brain>bone>CSF>eye |
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Azole MOA
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inhibition of 14-alpha-demethylase causes inhibition of ergosterol synthesis resulting in accumulation of toxic sterols in the cell membrane
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Echinocandins MOA
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inhibition of beta-1,3 glucan synthase causing inhibition of beta- 1,3 & beta-1,6 glucans synthesis causing fungal cell walls to become structurally abnormal and susceptible to osmotic stress
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Isoniazid MOA
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acylates NADH and prevents if from reducing alkene in FA synthesis ultimately blocking mycolic acid synthesis and disrupting the cell wall
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Rifampin MOA
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inhibits DNA-dependent RNA polymerase (DDRP):
-π-π bonding between naphthalene & aromatic amino acids of DDRP -chelation to Zn present in DDRP (OH @ C1 & C8) -hydrogen bonding to enzyme (OH @ C21 & C28) |
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Ethambutol MOA
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-inhibition of arabinosyl transferase which ultimately inhbits LAM and AG destroying integrity of cell wall
-blocks RNA synthesis |
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Pyrazinamide MOA
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-lowers pH of media
-antimetabolite of NAD synthesis which is necessary for FA synthesis -inhibits the gene that endocdes for FA synthase I thus inhibiting FA synthesis |
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Streptomycin MOA
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inhibits protein synthesis by binding to the 30S ribosomal subunit
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Causes of Community Acquired Pneumonia
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1. Streptococcus pneumoniae
2. Haemophilus influenzae 3. Moraxella catarrhalis |
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Capsid Virus
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-capsid
-environmentally stable -released via cell lysis -easily spread via oral or fecal route -can dry out & retain infectivity -can survive GI -elicit protective antibody response |
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Envelope Virus
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-envelope membrane
-environmentally liable released via cell lysis & budding -must stay wet to remain infectious -do not survive GI -spread via blood, body secretions, & transplants -elicit cell-mediated immune response or hypersensitivity & inflammation response |
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Uncoating Inhibitors MOA
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neutralize and inhibit Influenza A viral uncoating preventing virus from penetrating host cells
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Ribavirin MOA
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causes alteration of cellular nucleotide pools and inhibition of viral mRNA synthesis
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"Cyclovirs" MOA
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activated via viral thymidine kinase and converted to a triphosphate derivative that inhibits DNA synthesis & viral replication by competeing with deoxyguanosine triphosphate for viral DNA polymerase becoming incorporated into vral DNA causing termination of DNA chain
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Nucleoside Analogs MOA
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inhibition of viral DNA replication similar to "Cyclovirs" with different nucleotide derivatives
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Non-Nucleosie Analogs MOA
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directly inhibits DNA polymerase
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Neuraminidase Inhibitors MOA
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N-acetylneuraminic acid (sialic acid) analog that inhibits viral neuraminidases & leaves uncleaved sialic acid residues on the surfaces of the host cells and influenza viral envelopes. Viral hemagglutinin binds these residues resulting in a viral aggregation at the host cell & a reduction in the amount of virus that is released to infect other cells.
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Interferons & Immunoglobulins MOA
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inhibition of viral penetration or uncoating, synthesis of mRNA, translation of viral proteins, &/or viral assembley and release
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Sulfonamides MOA
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antimetabolite of PABA
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Trimethoprin MOA
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antimetabolite of dihydrofolic acid that inhibits dihydrofolate reductase
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Nitrofurans MOA
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-inhibits acetyl-CoA thereby interfering with carbohydrate metabolism
-dirsupts bacterial cell wall formation |
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Methenamine MOA
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causes denaturation of proteins by forming a Schiff base
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Fosfomysin MOA
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-analog of fosfoenopyruvate that acts as a false substrate of transferase and inhibits peptidoglycan and cell wall synthesis
-decreases affinity of bacteria to cell wall (?) |
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Phenazopyridine MOA
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urinary analgesic with NO antimicrobal properties
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Undecylenic Acid MOA
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alters membrane and conditions needed for fungal growth
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Talnaftate MOA
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blocks the oxidation of squalene to squalene epoxidase and ultimatley the formation of ergosterol
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Allylamines MOA
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interfere with ergosterol synthesis by blocking squalene-2,3 epoxidase
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Ciclopirox MOA
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-blocks fungal transmembrane transport
-interferes with DNA & RNA synthesis |
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Griseofulvin MOA
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inhibits mitosis by interacting with microtubules causing disruption of the mitotic apparatus arresting metaphase
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Flucytosine MOA
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inhibits DNA synthesis by inhibiting thymidylate synthase which converts uracil into thymine
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MAC drug therapy
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-Macrolides (Clarithroymcin, Azithromycin)
-Refabutin -Ethambutol -Ciprofloxacin -Clofazimine |
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Ethionamide MOA
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acylated InhA (NAD) leading to inhibition of FA synthesis
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Para-aminosalicylic acid (PAS) MOA
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antimetabolite of PABA
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Cycloserine MOA
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inhibitor of L-alanine racemase that converts L-alanine into D-alanine ultimately inhibiting synthesis of peptidoglycan needed for the cell wall
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Capreomycin MOA
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inhibits protein synthesis by binding to the 50S ribosomal subunit
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Kanamycin MOA
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inhibits protein synthesis by binding to the 30S ribosomal subunit
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